风湿性心脏病心房颤动患者心房组织碱性成纤维细胞生长因子及转化生长因子β_1的表达及意义

Expression and significance of bFGF and TGF-β1 in atrial tissue of patients with atrial fibrillation*

目的观察风湿性心脏病(风心病)心房颤动(房颤)患者心房组织中碱性成纤维细胞因子(bFGF)及转化生长因子β1(TGF-β1)的表达情况,并探讨其在风心病房颤心房纤维化中的作用及意义。方法将38例风心病二尖瓣病变接受换瓣手术者于术中获取的右心耳分为3组,其中窦性心律组8例,阵发性房颤组10例,持续性房颤组大于或等于6个月20例。应用羟脯氨酸含量测定法检测各组心房组织胶原含量;应用免疫组织化学技术检测各组心房组织中bFGF和TGF-β1的蛋白表达及分布。结果bFGF和TGF-β1主要表达在心肌细胞的胞质;与风心病窦性心率组相比,bFGF和TGF-β1表达及胶原含量在阵发性和持续性房颤组均显著增加(P<0.01);与阵发性房颤组相比,持续性房颤组中这两种细胞因子的表达及胶原含量继续明显增加(P<0.05)。bFGF和TGF-β1与胶原含量进行相关分析,发现bFGF及TGF-β1的表达程度与心房胶原含量均呈正相关,即随心房胶原含量的增加,bFGF(r=0.52,P<0.05)、TGF-β1(r=0.70,P<0.01)表达增强。结论风心病患者心房组织中bFGF和TGF-β1的表达上调可能是心房纤维化发生的分子机制之一,在风心病房颤的发生和维持中可能起重要作用。

Objective To investigate the expressive feature of bFGF and TGF-β1 in atrial tissue of the patient with rheumatic heart disease（RHD） ,and the effects of bFGF and TGF-β1 on rheumatic atrial myocardial fibrosis. Methods Of 38 RHD patients,8 were with sinus rhythm, 10 were with paroxysm atrial fibrillation （pAF）,and 20 with chronic AF（cAF） （≥6 months）. The right atrial muscle specimens were obtained during the operation on mitral valve replacement. The collagen content of myocardium specimens was obtained hy hydroxyproline detection; the expression and distribution of bFGF and TGF-β1 were examined by immunohistochemical stain. Imaging analysis was employed to measure the degree of immunohistochemical staining. Results RHD atrial myocardium showed high content of collagen. Both bFGF and TGF-β1 were stained major in myocardium cells. Both of the collagen content and bFGF or TGF-β1 expression in pAF group and oAF group were stronger than those in sinus rhythm group （P〈0.01） ; cAF group was stronger than that in pAF group （P〈0. 05）. The positive expression degree of bFGF and TGF-β1 in RHD was in creased and correlated positively with the content of myocardial collagen （bFGF：r=0.52,P〈0.05; TGF-β1：r=0.70,P〈0.01 ）. Conclusion The expression of bFGF or TGF-β1 in human atria may have correlation with the initiation or maintenance of AF,and may contribute as a molccular mechanism for the development of atrial fibrosis in the patients with RHD,which produces a struc tural basis for AF.